The Role of Mitochondria in Reactive Oxygen Species Metabolism and Signaling

By A. A. Starkov. Annals of the New York Academy of Sciences, 2008

817 citations recorded by the source corpus.

Oxidative stress is considered a major contributor to the etiology of both “normal” senescence and severe pathologies with serious public health implications. Several cellular sources, including mitochondria, are known to produce significant amounts of reactive oxygen species (ROS) that may contribute to intracellular oxidative stress. Mitochondria possess at least 10 known sites that are capable of generating ROS, but they also feature a sophisticated multilayered ROS defense system that is much less studied. This review summarizes the current knowledge about major components involved in mitochondrial ROS metabolism and factors that regulate ROS generation and removal at the level of mitochondria. An integrative systemic approach is applied to analysis of mitochondrial ROS metabolism, which is “dissected” into ROS generation, ROS emission, and ROS scavenging. The in vitro ROS‐producing capacity of several mitochondrial sites is compared in the metabolic context and the role of mitochondria in ROS‐dependent intracellular signaling is discussed.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5e782af7af080ce2ab1918eaf750eed5607d64ed

How researchers see this paper

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In Molecular Biology

1. M. Juhaszova
2. D. Granger
3. P. Kvietys
4. D. Zorov
5. Steven J. Sollott
6. P. Shaw
7. S. Barber
8. C. Giorgi

In Physiology

1. P. Shaw
2. D. Granger
3. S. Barber
4. M. Juhaszova
5. P. Kvietys

Citations in the corpus

• Mitochondrial DNA mutations and human disease. (2010, background): “They are the major source of endogenous reactive oxygen species (ROS) [4] and they host other important biochemical pathways, including the tricarboxylic acid (TCA) cycle and parts of the urea cycle [5].”
• Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “At least, ten mammalian mitochondrial enzymes contribute to ROS production [17, 19] even if their capacity of ROS producing greatly differ in a tissues-specific manner [20].”
• ROS and ROS-Mediated Cellular Signaling (2016, background): “bacterial invasion, that generate ROS intentionally, either in molecular synthesis or in breakdown, as part of a signal transduction pathway, or as part of a cell defense mechanism [10– 12].”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “Mitochondria can be both a source and a target of ROS (reviewed in Starkov, 2008 and Murphy, 2009).”
• Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “Mitochondrial-specific antioxidant mechanisms do exist, including SOD1, SOD2 (manganese SOD), glutathione peroxidases, and peroxiredoxin 3, which are usually able to combat the high rate of ROS production [112].”
• Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “erates O2 ·− is by RET via complex II; usually requiring succinate as a substrate [305,308].”
• Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “Good reviews on the current mechanisms of ROS production in mitochondria are available elsewhere for the reader interested in a general background and for those interested in substantially detailed mechanistic depth (3, 13, 201, 202, 308, 397, 416).”
• Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases (2014, background): “The other mitochondrial components which contribute to the formation of ROS include monoamino oxidase, aketoglutarae dehydrogenase, glycerol phosphate dehydrogenase and p66shc [64].”